Skin abscess with lumbar epidural catheterization in infants: is it dangerous? Report of two cases.
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Publications and source records attributed to C Ecoffey.
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This randomized prospective study measured the effects of an intravenous opioid bolus on cerebrospinal fluid pressure (CSFP), mean arterial pressure (MAP), and cerebral perfusion pressure (CPP) during skull-pin insertion. Twenty-two adult patients scheduled for elective craniotomy for supratentorial lesions were studied. Outcome variables were MAP, heart rate (HR), and lumbar CSFP. The standardized anesthetic regimen included fentanyl (2 microg/kg), thiopental (5-7 mg/kg), lidocaine (1.5 mg/kg), isoflurane (0.3-0.7 minimum alveolar anesthetic concentration), and vecuronium (0.1 mg/kg). During stable anesthesia, sufentanil (0.8 microg/kg) or fentanyl (4.5 microg/kg) was given as a bolus before skull-pin insertion. The hemodynamic effects of the opioid injection were modified with phenylephrine and/or atropine when indicated. CSFP remained unchanged in both treatment groups. MAP and CPP increased approximately 10 mm Hg after skull-pin insertion (P<0.001). In the sufentanil group, HR decreased approximately 10 bpm after opioid injection and remained decreased throughout the study. In fentanyl-treated patients, HR decreased 8 bpm after opioid injection but returned to preopioid rates after skull-pin insertion. In conclusion, in anesthetized patients, an intravenous bolus of fentanyl or sufentanil prior to skull-pin insertion results in stable values of CSFP, CPP, BP, and HR when the hemodynamic effects of the opioid are modified with phenylephrine and atropine.
BACKGROUND: During orthotopic liver transplantation (OLT), acute depression of myocardial contractility has been suspected at the time of the graft reperfusion. METHODS: The authors tested the hypothesis that plasma collected at the time of reperfusion in OLT patients exerted a negative inotropic effect on isolated rat myocardium. Plasma from 13 OLT patients was collected either before surgical incision (group 1, n = 8) or 3-5 min after vena cava and portal vein unclamping (group 2, n = 9). Six patients had their pre- and postincision plasma analyzed. A postreperfusion syndrome was observed in 3 of 13 patients. Left ventricular rat papillary muscles were studied at baseline (T0), 30 min after the addition of plasma (T30), and 60 min after the addition of plasma (T60). The authors recorded contraction parameters (maximum unloaded shortening velocity [Vmax], peak extent of systolic shortening at preload [deltaL], maximum active isometric tension [AFi], positive peak tension derivative [+dFi/dt], time-to-peak shortening [TPS], and time-to-peak force [TPF]) and relaxation parameters (maximum lengthening velocity at preload [VI], negative peak tension derivative [-dFi/dt], index of load sensitivity of relaxation [tRi]). RESULTS: In group 1, contraction parameters remained unchanged, with the exception of a decreased Vmax at T30 and AFi at T60 (each P < 0.05). In group 2, all contraction parameters were significantly decreased at T30 and at T60, with the exception of AFi at T60. Both types of plasma decreased V1 and altered tRi at T30 and T60, whereas only reperfusion plasma decreased -dFi/dt at T30 and T60. At T30, deltaL, -dFi/dt, and tRi were significantly more impaired in group 2 than in group 1. There was no relationship between inotropic changes and mean arterial pressure decrease at the time of reperfusion. CONCLUSION: Plasma collected at the time of graft reperfusion in OLT patients exerted negative effects on contraction and relaxation performance in isolated rat left ventricular papillary muscle.
BACKGROUND: The cardiovascular side effects of volatile anesthetics are one of the chief causes of postoperative complications in children, and infants seem to be at the greatest risk for this. This study compared cardiovascular changes at equipotent concentrations of sevoflurane and halothane in infants. METHODS: Thirty infants classified as American Society of Anesthesiologists physical status I or II who required elective surgery were randomized to receive either halothane or sevoflurane for inhalation induction. Cardiovascular and echocardiographic data were recorded in both groups at baseline and at end-tidal concentrations of 1 and 1.5 minimum alveolar concentration (MAC). RESULTS: Sevoflurane did not alter heart rate or cardiac index at all concentrations compared with awake values. Sevoflurane significantly decreased blood pressure and systemic vascular resistance compared with awake values at all concentrations. Shortening fraction and rate-corrected velocity of circumferential fiber shortening decreased at 1.5 but not at 1 MAC. Myocardial contractility assessed by stress-velocity index and stress-shortening index decreased significantly at all concentrations, but did not fall into the abnormal range at any concentration. Halothane caused a greater decrease in heart rate, shortening fraction, stress-shortening index, velocity of circumferential fiber shortening, stress-velocity index, and cardiac index at all concentrations than did sevoflurane. CONCLUSION: Sevoflurane causes a lesser decrease in cardiac output than does halothane in infants.
Clinical and echocardiographic haemodynamic evaluations of response to volume expansion are described in 12 preterm neonates aged < 7 days presenting without cardiac dysfunction and with a low cardiac output. They received 10% albumin solution (20 ml kg-1) for 3 h. Measurements were made before infusion, at volumes 5, 12.5 and 20 ml kg-1 and 1 h later. All infants increased significantly their cardiac output (CO) (from a median of 177 to 283 ml kg-1 min-1). The rise of CO decreased with the volume infused. The index of systemic vascular resistance (SVR = ratio of mean arterial pressure to the CO) decreased for the six patients without PDA (from 272 to 193 mmHg l-1 kg-1 min-1, p < 0.05) showing that the hypovolaemic preterm infant is able to shut down peripherally in response to hypovolaemia. The four hypotensive infants responded by increasing mean arterial blood pressure (from 29 to 44 mmHg). Cutaneous refilling time decreased during infusion (from 6.7 to 3.8 s. p < 0.01). One infant had an haemodynamically significant ductus arteriosus revealed by volume expansion, another one developed myocardial dysfunction.
Efficient and prolonged postoperative analgesia is obtained with regional anesthesia in pediatrics. Its wide use has been due to an easy performance in pediatrics with a success rate near 100% for the peripheral blocks, and to a minimal deleterious hemodynamic effect of the sympathetic block following an epidural anesthesia. Regional anesthesia in pediatrics have many indications and few contra-indications. In addition the risk of accidents is low and was observed mainly with perimedullar blocks.
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OBJECTIVES: To compare the preventive effects of esmolol and lidocaine on the increase in mean arterial pressure (MAP) and intracranial pressure (ICP) during endotracheal intubation in neurosurgery. STUDY DESIGN: Comparative, randomised, double-blind study. PATIENTS: Twenty-two patients, physical status ASA I or II, undergoing neurosurgery, and randomised into two groups (esmolol group and lidocaine group). METHODS: After induction of anaesthesia with thiopentone, vecuronium, fentanyl and isoflurane, one group received iv esmolol 1.5 mg.kg-1 and the other iv lidocaine 1.5 mg.kg-1, 130 sec before endotracheal intubation. The MAP measured with a radial catheter, the ICP obtained with a lumbar subarachnoid catheter and the cerebral perfusion pressure (CPP, calculated from MAP and ICP) were assessed before induction of anaesthesia, before esmolol or lidocaine injection, and before intubation, during the maximal change in MAP, as well as 2 and 5 minutes after intubation. RESULTS: The time course of MAP, ICP and CCP were similar throughout the study in the two groups, with a significant decrease (P < 0.05) of the CPP from 92 +/- 12 to 62 +/- 8 mmHg after esmolol, and from 96 +/- 12 to 68 +/- 15 mmHg after lidocaine. Following intubation, CPP increased significantly (P < 0.05) to 99 +/- 23 mmHg after esmolol and to 99 +/- 17 mmHg after lidocaine. The ICP increased also significantly (P < 0.05) after intubation from 11 +/- 6 to 17 +/- 10 mmHg in the esmolol group, and from 10 +/- 6 to 16 +/- 9 mmHg in the lidocaine group. CONCLUSIONS: Esmolol or lidocaine as an iv bolus of 1.5 mg.kg-1 before laryngoscopy and intubation do not completely prevent the increase in MAP and ICP.
OBJECTIVE: As hydratation of the normal brain is much more dictated by osmotic gradients than by hydrostatic or oncotic pressures, this study aimed to compare the effect of the infusion of currently used volume loading solutions on plasma osmolality. STUDY DESIGN: Randomized, comparative trial. PATIENTS: Thirty ASA 1-2 patients, scheduled for lumbar intervertebral disc surgery were randomly allocated to three groups receiving either 2,000 mL of lactated Ringer's solution (RL, n = 10), 750 mL of hydroxyethylstarch 6% (HEA, n = 10) or 2,000 mL of normal saline (NaCl, n = 10). METHODS: Baseline osmolality, natraemia, glycaemia and protidaemia were measured before induction of anaesthesia (T1), after the infusion of 375 mL of hydroxyethylstarch or 1,000 mL of crystalloids (T2) and at the end of the infusion (T3). RESULTS: The three groups were identical for age, weight, initial plasma osmolality and natraemia. However, osmolality in the RL group was decreased at T2 and T3 compared to T1 (respectively: 299 +/- 5 mOsm.kg-1, 295 +/- 4 mOsm.kg-1 and 292 +/- 5 mOsm.kg-1. Osmolality at T2 and T3 was also lower in the RL group compared to the HEA and NaCl groups (respectively: 301 +/- 6 mOsm.kg-1 and 304 +/- 13 mOsm.kg-1 for T2 and T3 in the HEA group, and 299 +/- 5 mOsm.kg-1 and 298 +/- 5 mOsm.kg-1 in the NaCl group). In the HEA and NaCl groups, osmolality was unchanged at T2 and T3 compared to T1. CONCLUSION: Both normal saline and hydroxyethylstarch 6% maintain plasma osmolality, whereas Ringer lactate tends to decrease it. For that reason normal saline and hetastarch 6% but not lactated Ringer's solution, may be administered in patients experiencing blood-brain barrier damage.
Twenty-six patients requiring orthopaedic surgery were anaesthetized and oesophageal and rectal temperature were monitored continuously. Twenty patients requiring a pneumatic tourniquet were allocated prospectively to one of two groups: passive group (Pg) with reflective insulation on all available skin surface (n = 10) and forced group (Fg), with active warming by a forced air system (n = 10). Six patients without a tourniquet were used as a reference group (Rg). The pneumatic tourniquet time was similar in the tourniquet groups. During tourniquet inflation, oesophageal temperature increased with time. The difference was significant compared with the reference group at approximately 20 min. At about 30 min, oesophageal temperature in group Fg was significantly higher than that in group Pg. After tourniquet deflation, temperature decreased transiently. Changes in rectal temperature were similar but delayed significantly. A mechanism to explain the increase in core temperature during pneumatic tourniquet use remains unclear. A redistribution mechanism by cooling of the blood in a cold and vasodilated limb could explain the decrease of temperature after tourniquet deflation.
In many studies reporting an increase in cerebrospinal fluid pressure (CSFP) after opioid administration, concomitant decreases in mean arterial pressure (MAP) have been observed. Autoregulatory cerebral vasodilation may therefore have been a factor in the CSFP increases. We tested the hypothesis that increases in CSFP after bolus injection of opioids could be minimized by modifying concomitant decreases in MAP with phenylephrine. Thirty-three patients with supratentorial mass lesions were studied in a randomized, prospective, double-blind, saline-controlled comparative trial. The principal outcome measures were lumbar CSFP, MAP, and heart rate (HR). Study drugs, sufentanil 0.8 micrograms/kg (n = 12), fentanyl 4.5 micrograms/kg (n = 11), or normal saline (n = 10), were injected intravenously (IV) during stable general anesthesia with 0.3-0.7 minimum alveolar anesthetic concentration (MAC) of isoflurane in oxygen and controlled ventilation (end-tidal carbon dioxide 32-35 mm Hg). Phenylephrine 50-100 micrograms was injected IV when MAP decreased by more than 15% of initial values, and atropine 0.5 mg IV when HR decreased to less than 45 bpm. Opioid administration was associated with significant decreases in MAP, 21 +/- 9 mm Hg (mean +/- SD) in the sufentanil group and 16 +/- 7 mm Hg in the fentanyl group; P < 0.001. These decreases in MAP were of short duration (i.e., corrected with 1-2 min). Patients in the sufentanil group needed more phenylephrine than patients in the fentanyl group (170 +/- 89 micrograms vs 100 +/- 47 micrograms; P < 0.05). No significant change in the CSFP was seen in either the sufentanil (1 +/- 6 mm Hg) or fentanyl-treated patients (O +/- 2 mm Hg). No significant changes in MAP or CSFP were observed in the saline-treated patients. HR decreased after injection of either study drug (P < 0.01) but remained unchanged in the saline group. In summary, during stable anesthesia with isoflurane in oxygen, bolus injections of fentanyl or sufentanil, despite producing rapidly corrected mean decreases in MAP of 18% and 25%, respectively, were not associated with any change in CSFP.
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There have been few evaluations of the perioperative pharmacokinetics of antibiotics. Piperacillin (PPR) is a widely prescribed ureidopenicillin of established efficacy against enterobacteria and P. aeruginosa. The serum pharmacokinetics and perioperative safety of PPR were evaluated in 8 patients hospitalized for an orthotopic liver transplantation. The subjects were given a 60 mg/kg infusion of PPR once every 8 hours. PPR was assayed by HPLC and data were analyzed by a noncompartmental method. There were no adverse events during surgery. It seems that kinetics of PPR showed no variation during the anhepatic period. However, transplants notably modified the kinetics of PPR in comparison with data previously published in healthy volunteers. Trends were as follows: flattening of Cmax and prolongation of T1/2 (2.2 h vs 0.92 h). This phenomenon seems to be due to a marked increase in V(area) (44.0 1 vs 16.2 1) while C1 were similar. The increase in V(area) is probably the combined results of multiple factors including blood loss, vascular filling, combined prescription of vasoactive drugs, and, obviously, the surgical procedure itself. Concentrations of PPR were after 4 hours below (i.e. 5/8 patients) the MIC of P. aeruginosa (i.e. < or = 16 micrograms/ml). From 6 hours onwards antibacterial cover was insufficient against the majority of enterobacteria (i.e. < or = 8 micrograms/ml). This inadequate protection included the critical anhepatic period. Measured concentrations achieved by the initial dosage regimen were compared to those obtained by simulation using modified dosing pattern in order to ensure circulating levels constantly of 16 micrograms/ml or more. This leads to a suggested modified dosage pattern in which PPR would be given as 1 dose of 60 mg/kg every 4 hours. Under these conditions the expected concentrations should be constantly over 16 micrograms/ml and any risk of systemic accumulation is excluded.
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Infection is the main complication of external ventricular drainage (EVD). This retrospective study assessed the relationships between EVD duration, antibiotics and cerebrospinal fluid (CSF) infection. From January 1990 to December 1991, 53 neurosurgical patients, aged 7-76 years, a simplified acute physiological score (SAPS) of 1-20 and having a total of 64 EVD, were included in this study. CSF withdrawn from the drain was collected daily for bacteriological, biochemical and cytological analysis, until the EVD removal. CSF colonization was defined by a positive direct examination or a positive culture of CSF, in the absence of biochemical and cytological abnormalities. CSF drain infection was defined by a low glucose concentration or leucocytosis without blood contamination. However the results of bacteriological analysis were modified by the antibiotics. The group of non infected patients and the group of those with an infected or a colonized drain were comparable with regard to underlying neurosurgical diseases, age, SAPS, Glasgow coma scale and delay between hospital admission and day of drain insertion and antibiotic administration. The EVD duration was significantly longer in infected EVD and colonized EVD. Staphylococci were the most frequently recognized bacteria and coagulase-negative staphylococci predominated in CSF of colonized EVD. In five patients, antibiotics were unable to cure a meningitis. Their leucocyte count was increased. The glucose concentration was low, but the culture, remained negative. It is concluded that duration and rate of EVD influence more the incidence of infections than the systemic administration of antibiotics.
A questionnaire completed by 90 adults after ENT or stomatological surgery showed that most of them were anxious preoperatively, mainly because of anaesthesia and that a "personalized" preanaesthetic examination was the most efficient means to decrease it. Although a majority of them was satisfied with the anaesthetic care, anaesthetic morbidity remains important. The personalization of pre, per and postanaesthetic management by the same anaesthetist is probably the best means for improving the quality of care.
Large prophylactic doses of aprotinin efficiently reduce blood loss during orthotopic liver transplantation (OLT). Small doses of aprotinin are usually used to treat fibrinolysis. However, no studies have investigated the benefit of prophylactic administration of a smaller dose of aprotinin during liver transplantation. We compared two methods of aprotinin therapy on transfusion outcome in liver transplant patients in a prospective study of 199 patients undergoing OLT who were randomized to large or small prophylactic doses of aprotinin during the transplant procedure. In the large-dose group (n = 94) an initial dose of 2,000,000 kallikrein inactivation units (KIU) was followed by infusion of 500,000 KIU/h until the patient's return to the intensive care unit. In the small-dose group (n = 95), an initial dose of 500,000 KIU was followed by an infusion of 150,000 KIU/h. Outcome measurements included intraoperative transfusion requirements (packed red blood cells, fresh frozen plasma, platelets, intraoperative salvage) and postoperative hematologic values. There were no differences in transfusion requirements in the two groups of patients. Patients treated with low-dose aprotinin had slightly higher postoperative fibrinogen concentrations. Large-dose aprotinin therapy does not appear to offer additional benefit compared to low-dose aprotinin administration.